Despite major developments in both diagnosis and treatment, cardiac-related disorders, such as heart failure (HF), continue to be a leading cause of death and disability in older adults worldwide and affect more than 12 million patients in the United States and Europe alone (Lloyd-Jones et al. (2010) Circulation 121:948-954). Until recently, HF therapy usually consisted of pharmacological approaches to counter maladaptive neurohormonal stimulation and restore favorable hemodynamics. Over the past decade, however, the major advance has come from a device therapy termed cardiac resynchronization therapy (CRT) that uses electrical pacing of both right and left ventricles to restore contraction timing. It is designed to counter the dyssynchronous contraction within the left ventricle stemming from electrical conduction delay that is found in nearly a third of patients with HF. Electromechanical dyssynchrony confers independent risks for worsened morbidity and mortality, and CRT improves both in affected patients (Cleland et al. (2005) N. Engl. J. Med. 352:1539-1549; Cleland et al. (2006) Eur. Heart J. 27:1928-1932; Bristow et al. (2004) N. Engl. J. Med. 350:2140-2150; and Abraham et al. (2002) N. Engl. J. Med. 346:1845-1853). CRT is unique among HF treatments because it both acutely (Kasser et al. (1999) Circulation 99:1567-1573) and chronically (St. John Sutton et al. (2009) Circulation 120:1858-1865) enhances systolic function of the heart, yet confers long-term survival benefits (Cleland et al. (2005) N. Engl. J. Med. 352:1539-1549 and Cleland et al. (2006) Eur. Heart J. 27:1928-1932). None of the commonly used drugs designed to stimulate ventricular pump function has yet achieved this. To date, however, knowledge of the molecular and cellular effects of CRT remains limited. Accordingly, there exists a need in the art to identify specific molecular modifications from CRT that can be used to target and treat HF more broadly, for example, in patients without dyssynchrony.